Kidney urine formation

The essential element, hypoperfusion of vital organs, is present whatever the cause, whether pump failure (myocardial infarction), maldistribution of blood (septic shock) or loss of total intravascular volume (bleeding or increased permeability of vessels damaged by bacterial cell products, bums or anoxia). Fimction of vital organs, brain (consciousness, respiration) and kidney (urine formation) are clinical indicators of adequacy of perfusion of these organs. 

Antidiuretic hormone (ADH), also referred to as vasopressin, has two major effects, both of which are reflected by its names (1) antidiuresis (decrease in urine formation by the kidney) and (2) vasoconstriction of arterioles. 

The presence of Ca in kidney stones and the abnormally high Ca levels in idiopathic (absorptive) hypercalciuric individuals that are inherently more prone to kidney stones, initially led to the belief that dietary Ca may be a cause of renal stone formation (Coe et al., 1992). Recent evidence suggests that, as a therapeutic approach to reducing the risk for kidney stones, Ca-restricted diets may pose a greater risk to normocalciuric individuals prone to kidney stone formation such an approach may increase urinary oxalate and the likelihood of recurrent stones, as well as promote bone loss (Borghi et ah, 2002 Coe et al., 1997 Curhan et ah, 1997). The amoimt of oxalate excreted in urine has been foimd to be positively associated with Ca oxalate supersaturation and stone formation (Holmes et ah, 2001). While free oxalic acid is readily absorbed from the gut lumen (Morozumi et ah, 2006), an increased dietary Ca to oxalate... 

When carbonic anhydrase inhibitors block the enzyme in the kidney, HjCOj formation— and consequently the availability of H3O+ (i.e., protons)—decreases. Since the Na+ ions in the filtrate cannot be exchanged, sodium is excreted, together with large amounts of water, as a result of ion hydration and osmotic effects. The result is diuresis, accompanied by a dramatic increase in urine volume. There is also failure to remove HCOj" ions because there is no H3O+ to form HjCOj, which would decompose to COj -1- HjO. Therefore, the normally slightly acidic urine becomes alkaline. The strong carbonic anhydrase inhibitors also increase K+ excretion, an undesirable effect. 

Diuretics are the agents which increase the rate of urine formation by the kidneys, or which cause a net loss of sodium and water in urine, i.e. the diuretics increase the urine output of ions and fluids from the kidneys. 

The most potent type of diuretic, loop diuretics are named after the loop of Henle, a component of a nephron. The nephrons are the filtering units of the kidney, and are responsible for moving fluids and waste out of the bloodstream, resulting in urine formation. The loop of Henle is a branch within each nephron where sodium and potassium are reabsorbed back into the bloodstream instead of being filtered into the urine. Loop diuretics inhibit this action and promote excretion of the sodium and potassium instead, along with calcium and magnesium. Since excess sodium causes excess fluid build-up, this results in fluid loss. Furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), and ethacryinic acid (Edecrin) are all loop diuretics. 

Figure 12.1 illustrates the main structure of a nephron [1], The measurements to be reported in this chapter were performed on rats. A rat kidney contains approximately 30000 nephrons as compared to the one million nephrons in a human kidney. The process of urine formation starts with the filtration of plasma in the glomerulus, a system of 20-40 capillary loops. The presence of a relatively high hydrostatic pressure in this system allows water, salts and small molecules to pass out through the capillary wall and into the proximal tubule. Blood cells and proteins are retained, and the filtration process saturates when the protein osmotic pressure balances the hydrostatic pressure difference between the blood and the filtrate in the tubule. For superficial nephrons, the proximal tubule is visible in the surface of the kidney and easily accessible for pressure measurements by means of a thin glass pipette. 

Dilution of the ECF reduces the thirst sensation and reduces ADH production so that normally the kidney produces diluted urine and eliminates the extra water. However, following rapid dehydration, the reduction in blood volume decreases cardiac output and BP, causing reflex vasoconstriction and reduced perfusion of tissues, including the kidney. This in turn reduces GFR and urine formation (oliguria) and the water is retained in the body. 

Figure 45-16 Diagrammatic representation of the interplay of factors involved in kidney stone formation. High or low pH may act as a promoter or inhibitor of stone formation depending on the stone type in question (e.g., calcium stone formation is favored by inadequate acidification while urate is less soluble in acidic urine). Controversy exists as to whether formed stones become trapped as they pass through the nephron ( free particle theory ) or whether stone formation occurs at damaged sites on the tubule wall ( fixed particle theory ).

Another important regulatory mechanism for urine formation is antidiuretic hormone (ADH), also known as vasopressin, which is released from the posterior pituitary in response to reduced blood pressure and elevated plasma osmolality. In the kidney, ADH acts on the collecting tubule to increase water permeability and reabsorption. As a result, the urine becomes more concentrated, and water is conserved in the presence of ADH. 

Two human genetic diseases are known which involve this disulphide amino acid. In one, cystinuria , there is a transport defect in the intestine and kidney. This results in abnormally high levels of cystine in the urine and can result in the precipitation of cystine crystals and kidney stone formation. In cystinosis, cystine crystals form within cells and eventually cause severe kidney damage. The nature of the primary biochemical lesion is unknown all known cystine reduction systems of the cell appear to be normal. 

Convoluted Tubule, Loop of Henle, and Urine Formation Reabsorption and Secretion in the Kidney 545... 

The main function of the kidney is urine formation. Urine is composed of water and solutes normally found in the blood. 

Symptoms of metabolic acidosis, besides low blood pH and high levels of H2CO3, include the following hyperventilation as the respiratory center tries to get excess CO2 out of the lungs, increased urine formation as the kidneys try to remove excess acids, thirst (to replace urination water loss), drowsiness, headache, and disorientation. The treatment again... 

FHtration is the initial step in urine formation. Of the plasma reaching the kidney, 20% is filtered by the selectively pemneable glomerular membrane. The resultant fluid is passed into Bowman s capsule. 

Two nucleation processes important to many people (including some surface scientists ) occur in the formation of gallstones in human bile and kidney stones in urine. Cholesterol crystallization in bile causes the formation of gallstones. Cryotransmission microscopy (Chapter VIII) studies of human bile reveal vesicles, micelles, and potential early crystallites indicating that the cholesterol crystallization in bile is not cooperative and the true nucleation time may be much shorter than that found by standard clinical analysis by light microscopy [75]. Kidney stones often form from crystals of calcium oxalates in urine. Inhibitors can prevent nucleation and influence the solid phase and intercrystallite interactions [76, 77]. Citrate, for example, is an important physiological inhibitor to the formation of calcium renal stones. Electrokinetic studies (see Section V-6) have shown the effect of various inhibitors on the surface potential and colloidal stability of micrometer-sized dispersions of calcium oxalate crystals formed in synthetic urine [78, 79]. 

In addition to being involved in the formation of urine, the kidney acts as an endocrine organ secreting renin, erythropoietin, prostaglandins (qv), and kinins it is also capable of synthesizing substances such as la,25-dihydroxycholecalciferol [32222-06-3] One of the principal functions of the... 

PTH is the most important regulator of bone remodelling and calcium homeostasis. PTH is an 84-amino acid polypeptide and is secreted by the parathyroid glands in response to reductions in blood levels of ionised calcium. The primary physiological effect of PTH is to increase serum calcium. To this aim, PTH acts on the kidney to decrease urine calcium, increase mine phosphate, and increase the conversion of 25-OH-vitamin D to l,25-(OH)2-vitamin D. PTH acts on bone acutely to increase bone resorption and thus release skeletal calcium into the circulation. However, due to the coupling of bone resorption and bone formation, the longer-term effect of increased PTH secretion is to increase both bone resorption and bone formation. 

Administration of dibutyltin dichloride intraperito-neally to rats led to the formation of butyl(3-hydroxy-butyl)tm, butyl(4-hydroxybutyl)tin, and monobutyltin. The major metabolite (buty 1(3-hydroxybutyl)tin) was distributed to the kidney at a relatively high concentration compared with the other metabolites, and its concentration increased with time. Butyl(4-hydroxybutyl)tin was found in urine only. The parent compound and other metabolites were detected in the brain (Ishizaka et al., 1989). Dibutyltin diacetate was destarmylated by 14% within 90 h following a single oral dose in mice at 1.1 mg/kg body weight, with several butyltin derivatives found in the liver or faeces (Boyer, 1989). 

Although hexachloroethane-induced hepatic damage can cause increases in serum levels of liver enzymes, these enzyme changes are not specific to hexachloroethane exposure (Fowler 1969b Weeks et al. 1979). In male rats, exposure to hexachloroethane is associated with the presence of granular and cellular casts in the urine (NTP et al. 1989). These effects are related to the formation of hyaline droplets in the male rat kidney. 

Interest in the nature of interactions between shortchain organic surfactants and large molecular weight macromolecules and ions with hydroxyapatite extends to several fields. In the area of carles prevention and control, surfactant adsorption plays an important role in the Initial states of plaque formation (1-5) and in the adhesion of tooth restorative materials ( ). Interaction of hydroxyapatite with polypeptides in human urine is important in human biology as hydroxyapatite has been found as a major or minor component in a majority of kidney stones ( 7). Hydroxyapatite is used in column chromatography as a material for separating proteins (8-9). The flotation separation of apatite from... 

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